Abstract: This study aimed to explore the potential molecular mechanisms of methyl methacrylate (MMA) in the initiation and progression of asthma based on a network toxicology approach, providing theoretical evidence for the prevention and control of respiratory diseases related to occupational exposure. Potential targets of MMA were predicted using SwissTargetPrediction, STITCH, and SEA databases. Asthma-related targets were screened from GeneCards, OMIM, and CTD databases using “asthma” as the keyword, and overlapping targets were identified as candidate target genes. A protein-protein interaction (PPI) network was constructed using the STRING database, and core targets were screened via Cytoscape. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were subsequently performed. The results showed that ALB, EGFR, CYP19A1, CA9, and CA2 were potential core targets. GO analysis indicated that these targets were mainly involved in biological processes including cellular acid-base homeostasis, neurotransmitter signaling, and ion transport regulation. KEGG pathway analysis revealed significant enrichment in nitrogen metabolism and cellular homeostasis-related pathways. Molecular docking results further demonstrated stable binding interactions between MMA and the core target proteins, suggesting that MMA may induce airway microenvironment imbalance and inflammatory responses through modulation of the carbonic anhydrase system and EGFR signaling pathways. In conclusion, MMA may contribute to the occurrence and development of occupational asthma through a multi-target synergistic mechanism characterized by metabolic disorders, imbalance of acid-base homeostasis, and amplification of inflammatory responses. This research provides a theoretical basis for the prevention and control of respiratory diseases related to occupational exposure to MMA in dental settings.